A regulator of G protein signaling, RGS3, inhibits gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) secretion.
A regulator of G protein signaling, RGS3, inhibits gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) secretion.
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DOI：
10.1186/1471-2121-2-21
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Kehrl JH
中科院分区：
文献类型：
--
作者：
Neill JD;Duck LW;Sellers JC;Musgrove LC;Kehrl JH
脑下垂体前叶分泌的促黄体激素调节性腺功能。促黄体生成素的分泌既受促性腺激素对下丘脑促性腺激素释放激素反应性的改变调节，也受促性腺激素释放激素分泌的改变调节。决定促性腺激素反应的机制尚不清楚，但可能涉及G蛋白信号调节(RGSS)。这些蛋白通过拮抗或缩短Gα蛋白与磷脂酶Cβ等效应物的相互作用而发挥作用。此前，我们曾报道RGS3和促性腺激素释放激素受体cDNAs共转染COS细胞后，促性腺激素释放激素刺激的第二信使三磷酸肌醇的生成受到抑制。在这里，我们提出了RGS3抑制促性腺激素释放激素诱导的大鼠垂体细胞黄体生成素分泌的证据。在携带促性腺激素释放激素受体的COS细胞中，RGS3(RGS3T=RGS3314-519)比RSG3更有效地抑制促性腺激素释放激素刺激的三磷酸肌醇的产生。RSG3/谷胱甘肽-S-转移酶融合蛋白结合的35S-GQα比所测试的G蛋白家族的任何其他成员都多。腺病毒介导的RGS3基因转移抑制促性腺激素释放激素刺激的促黄体生成素分泌，并呈剂量依赖关系。Adeno-RGS3还抑制促性腺激素释放激素刺激的~3H-肌醇磷酸蓄积，这与Gqα蛋白的分子作用部位一致。RGS3通过结合和抑制Gqα蛋白功能的转导特性，明显抑制促性腺激素释放激素刺激的第二信使(三磷酸肌醇)的产生和促黄体激素的分泌。氨基端截短的RGS3在抑制促性腺激素释放激素刺激的三磷酸肌醇产生方面甚至比完整的RGS3更有效。
Luteinizing hormone secreted by the anterior pituitary gland regulates gonadal function. Luteinizing hormone secretion is regulated both by alterations in gonadotrope responsiveness to hypothalamic gonadotropin releasing hormone and by alterations in gonadotropin releasing hormone secretion. The mechanisms that determine gonadotrope responsiveness are unknown but may involve regulators of G protein signaling (RGSs). These proteins act by antagonizing or abbreviating interaction of Gα proteins with effectors such as phospholipase Cβ. Previously, we reported that gonadotropin releasing hormone-stimulated second messenger inositol trisphosphate production was inhibited when RGS3 and gonadotropin releasing hormone receptor cDNAs were co-transfected into the COS cell line. Here, we present evidence for RGS3 inhibition of gonadotropin releasing hormone-induced luteinizing hormone secretion from cultured rat pituitary cells. A truncated version of RGS3 (RGS3T = RGS3 314–519) inhibited gonadotropin releasing hormone-stimulated inositol trisphosphate production more potently than did RSG3 in gonadotropin releasing hormone receptor-bearing COS cells. An RSG3/glutathione-S-transferase fusion protein bound more 35S-Gqα than any other member of the G protein family tested. Adenoviral-mediated RGS3 gene transfer in pituitary gonadotropes inhibited gonadotropin releasing hormone-stimulated luteinizing hormone secretion in a dose-related fashion. Adeno-RGS3 also inhibited gonadotropin releasing hormone stimulated 3H-inositol phosphate accumulation, consistent with a molecular site of action at the Gqα protein. RGS3 inhibits gonadotropin releasing hormone-stimulated second messenger production (inositol trisphosphate) as well as luteinizing hormone secretion from rat pituitary gonadotropes apparently by binding and suppressing the transduction properties of Gqα protein function. A version of RGS3 that is amino-terminally truncated is even more potent than intact RGS3 at inhibiting gonadotropin releasing hormone-stimulated inositol trisphosphate production.
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影响因子：
64.5
作者：
Koelle, MR;Horvitz, HR
通讯作者：
Horvitz, HR
影响因子：
56.9
作者：
BELCHETZ, PE;PLANT, TM;KNOBIL, E
通讯作者：
KNOBIL, E
影响因子：
4.1
作者：
KREY, LC;KAMEL, F
通讯作者：
KAMEL, F
影响因子：
64.8
作者：
Druey, KM;Blumer, KJ;Kehrl, JH
通讯作者：
Kehrl, JH
影响因子：
4.8
作者：
HAWES, BE;CONN, PM
通讯作者：
CONN, PM